Gastric acid stimulation and production with GERD, PUD, and gastritis disorders. Jamie is a 3-month-old female who presents with her mother for evaluation of “throwing up.” Mom reports that Jamie has been throwing up pretty much all the time since she was born. Jamie does not seem to be sick. In fact, she drinks her formula vigorously and often acts hungry. Jamie has normal soft-brown bowel movements every day and, overall, seems like a happy and contented baby. She smiles readily and does not cry often. Other than the fact that she often throws up after drinking a bottle, she seems to be a very healthy, happy infant. A more precise history suggests that Jamie does not exactly throw up—she does not heave or act unwell—but rather it just seems that almost every time she drinks a bottle she regurgitates a milky substance. Mom thought that she might be allergic to her formula and switched her to a hypoallergenic formula. It didn’t appear to help at all, and now Mom is very concerned. Cas

Gastric acid stimulation and production with GERD, PUD, and gastritis disorders. Jamie is a 3-month-old female who presents with her mother for evaluation of “throwing up.” Mom reports that Jamie has been throwing up pretty much all the time since she was born. Jamie does not seem to be sick. In fact, she drinks her formula vigorously and often acts hungry. Jamie has normal soft-brown bowel movements every day and, overall, seems like a happy and contented baby. She smiles readily and does not cry often. Other than the fact that she often throws up after drinking a bottle, she seems to be a very healthy, happy infant. A more precise history suggests that Jamie does not exactly throw up—she does not heave or act unwell—but rather it just seems that almost every time she drinks a bottle she regurgitates a milky substance. Mom thought that she might be allergic to her formula and switched her to a hypoallergenic formula. It didn’t appear to help at all, and now Mom is very concerned. Cas

Gastrointestinal Tract: Disorders of Motility

Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis Disorders

“The road to health is paved with good intestines!” (Sherry A. Rogers). Gastric acid is generally produced in the stomach and is essential for digestion. Motility disorders are abnormal muscle and nerve contractions causing spasms or lack of motion anywhere along one’s gastrointestinal tract. The stomach, the small and the large intestine, as well as the colon and the rectum, may be unable to perform their functions in the digestive process. Gastrointestinal motility changes depending on feeding, and GI motility is divided into fasting and postprandial contract patterns (Kitazawa & Kaiya, 2019). This motility is controlled by the contractility of smooth muscles of the GI tract, extrinsic and intrinsic neurons and some hormones. This essay will explore the normal pathophysiology of gastric acid stimulation and production and changes occurring in gastric acid stimulation and production with GERD, PUD, and gastritis disorders. Lastly, look at how age impacts the pathophysiology of GERD, PUD, and gastritis.

The Normal Pathophysiology of Gastric Acid Stimulation and Production

Gastric Acid Stimulation

Parietal and proximal cells are located in the stomach and are responsible for secreting gastric acid. This acid plays a crucial digestive function by lowering the PH in the stomach, creating prime conditions for enzymes to act on the food. Gastric acid secretion is initiated in the mouth, with thought, smell and taste acting as vagal stimulants for the stomach’s G cells to start the secretion (Isackson & Ashley, 2020). The ingestion of proteins is also a stimulant increasing gastric production. As the production of gastric acid increases, the acid circulates within the digestive tract causing histamine release by enterochromaffin-like cells. The release of histamine acts on the H2 receptors located on the parietal cells leading to further PH reduction as more gastric acid is released.

Gastric Acid Production

Gastric acid production is an inherent ability of all people from birth through the secreted amounts only peak at two years of age. Peak acid production continues through childhood to old age, but acid production sometimes drops due to gastritis as a medical condition. For healthy people, the mucosa walls of the gastrointestinal tract produce mucus acting as a protection layer against the acid’s corrosion. This protection occurs through three main stages. Firstly, the production of mucus and hydrogen carbonate creates a pH gradient keeping the acid within the tract (Taherali et al., 2018). Secondly, epithelial cells lining the tract walls use their membrane transport system to extract hydrogen ions from the acid to neutralize it. Lastly, capillary blood vessels in the tract walls collect the acid that diffuses through the epithelial membrane and eliminates them from the tract. Such strategies may disturb the mucosal membrane and result in the development of peptic ulcer disease, gastroesophageal reflux disease, and other gastric disorders.

Changes that Occur to Gastric Acid Stimulation and Production with GERD, PUD, and Gastritis Disorders

Interfering with the production of the mucosal layer of the gastrointestinal tract causes gastric disorders, including peptic ulcer disease and gastroesophageal reflux disease, where helicobacter pylori infection and non-steroidal anti-inflammatory drugs interfere with mucosal membranes. H. pylori infection causes tears on the mucosal membrane, presented as ulcers and inflammation. Non-steroidal anti-inflammatory drugs affect the mucosal membrane through topical and systematic actions causing ulcers and inflammation (Fokunang et al., 2018). These drugs block cyclooxygenase enzyme action to inhibit prostaglandin production and suppress blood flow, mucus secretion, production of hydrogen carbonate, and cell repair and replication, all in the gastrointestinal tract. The drugs contain low pH and are non-ionized in gastric acid, hence easy diffusion across the tract’s walls and into the epithelial cells.

The Impact of Age on the Pathophysiology of GERD, PUD, and Gastritis

The pathophysiology of peptic ulcer disease and gastroesophageal reflux disease can be impacted by age, where in children, it is notable that they have an anti-reflux barrier whose function is to ensure frequent relaxations and retrograde flow of gastric contents into the esophageal sphincter barrier existing between the esophagus and stomach is impaired as a factor of age and immaturity among children (Khan & Orenstein, 2018). This condition is caused by the lower esophageal sphincter’s incomp